CSHL Cell Death Conference

CSHL细胞死亡会议

• 批准号: 9331209
• 负责人: DAVID J. STEWART
• 金额: $ 0.5万
• 依托单位: COLD SPRING HARBOR LABORATORY
• 依托单位国家: 美国
• 财政年份: 2017
• 资助国家: 美国
• 起止时间: 2017-04-01 至 2018-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9331209
• 关键词: Acquired Immunodeficiency Syndrome; Address; Aging; American; Animals; Apoptosis; Apoptotic; Area; Asians; Atypical lymphocyte; Autoimmunity; Autophagocytosis; BCL2 gene; Biochemical Pathway; Biochemical Process; Biochemical Reaction; Biochemistry; Biological Assay; Biological Models; Cell Count; Cell Cycle Regulation; Cell Death; Cell physiology; Cells; Cellular Structures; Cellular biology; Cessation of life; Communicable Diseases; DNA Damage; Dangerousness; Data; Development; Developmental Biology; Diné Nation; Disease; Ensure; Environment; European; Faculty; Fostering; Genes; Genetic; Genomic approach; Goals; Health; Homeostasis; Human; Immunology; Industrialization; International; Invertebrates; Investigation; Ischemic Stroke; Laboratories; Length of Stay; Link; Lower Organism; Malignant Neoplasms; Mammals; Mitochondria; Molecular; Molecular Biology; Mutagenesis; Neurobiology; Neurodegenerative Disorders; Oral; Organism; Participant; Pathology; Pathway interactions; Plants; Play; Postdoctoral Fellow; Process; Protein Family; Published Comment; Quality Control; Receptor Signaling; Regulation; Regulator Genes; Research Institute; Research Personnel; Role; Schedule; Science; Scientist; Seasons; Selection Criteria; Senior Scientist; Series; Stroke; Structure; Suppressor Genes; System; Therapeutic; Tissues; Transcriptional Regulation; Tumor Suppressor Genes; Virus; Virus Diseases; Woman; Work; accomplished suicide; age related; biophysical techniques; cancer therapy; cell suicide; gene product; graduate student; interest; killings; lectures; meetings; neoplastic cell; neuron loss; novel; novel therapeutic intervention; posters; programs; receptor; reconstitution; response; senescence; structural biology; success; symposium; translational approach; tumor progression; tumorigenesis; unpublished works

Abstract Cold Spring Harbor Laboratory Conference on Cell Death August 15 - 19, 2017 The field of cell death encompasses many molecular and biochemical processes that were evolutionarily selected to promote self-elimination of cells. Programmed cell death is required for normal development and tissue homeostasis. Abnormalities in the regulation of cell death contribute to a wide variety of human disorders, including cancer, AIDS, stroke, autoimmunity and neurodegenerative disorders. Most if not all cells have the capacity to commit suicide, and key components of various cell death programs have been conserved in lower organisms, thereby providing powerful model systems for study. Some of the genes that regulate programmed cell death include oncogenes and tumor suppressor genes, providing a link between deregulation of cell death pathways and cancer. Many viruses encode genes that promote or inhibit cell death, indicating that subversion of this cellular process is an aspect of the pathology of virus infections. Rapid advancements in recent years have led to the identification of numerous genes and gene products involved in controlling different aspects of cellular death, and the biochemical pathways that regulate cell death have begun to emerge. New evidence strengthens the link between cell death mechanisms and mitochondrial energetics. Model systems have permitted directed mutagenesis of cell death regulatory genes mammals, invertebrates and lower organisms, demonstrating the role of cell death in a wide range of cellular responses and disease states. The development of cell-free assays and the reconstitution of biochemical reactions from purified components have served to delineate some of the details of cell death pathways. Researchers in the field of cell death are a diverse group whose interests span invertebrate to mammalian developmental biology, neurobiology, tumorigenesis, immunology, infectious diseases, biochemistry, cell biology, structural biology, cell cycle control, transcription regulation, receptor signaling and DNA damage pathways. The CSHL conference on Cell Death will be held on August 15 - 19, 2017. The objective of this conference is to bring together researchers working in the diverse aspects of programmed cell death and to facilitate new discoveries. The meeting plan includes an opening address, eight plenary and two poster sessions, in which participation by junior scientists will be facilitated. The overall goal is to create a meeting environment suitable for the open exchange of information and ideas that will foster advancement of the field toward a full understanding and development of new therapeutic approaches.

抽象的 冷春港实验室关于细胞死亡的实验室会议 2017年8月15日至19日 细胞死亡领域涵盖了许多分子和生化过程，这些过程在进化上是 被选为促进细胞的自我灭绝。正常开发和 组织稳态。细胞死亡调节的异常有助于多种人类 疾病，包括癌症，艾滋病，中风，自身免疫性和神经退行性疾病。大多数（如果不是全部） 细胞具有自杀的能力，各种细胞死亡程序的关键组成部分已经 在较低的生物体中保守，从而提供强大的研究模型系统。一些基因 调节程序性细胞死亡包括致癌基因和肿瘤抑制基因，提供了联系 细胞死亡途径和癌症的管制。许多病毒编码促进或抑制细胞的基因 死亡，表明这种细胞过程是病毒感染病理的一个方面。 近年来，快速发展导致了众多基因和基因产物的识别 参与控制细胞死亡的不同方面以及调节细胞的生化途径 死亡开始出现。新证据加强了细胞死亡机制与 线粒体能量学。模型系统允许定向细胞死亡调节的诱变 基因哺乳动物，无脊椎动物和较低的生物，证明了细胞死亡在广泛的 细胞反应和疾病状态。无细胞测定和重组的开发 来自纯化成分的生化反应已用于描述细胞死亡的一些细节 途径。细胞死亡领域的研究人员是一个多元化群体，其利益跨越无脊椎动物 哺乳动物发育生物学，神经生物学，肿瘤发生，免疫学，传染病， 生物化学，细胞生物学，结构生物学，细胞周期控制，转录调控，受体信号传导 和DNA损伤途径。 CSHL关于细胞死亡会议将于2017年8月15日至19日举行。 这次会议的目的是将研究人员聚集在一起 程序性细胞死亡并促进新发现。会议计划包括一个开幕词， 八个全体会议和两个海报会议将促进初级科学家的参与。这 总体目标是创建一个适合开放的信息和想法交换的会议环境 将促进该领域的进步，以充分理解和发展新的治疗性 方法。